OBJECTIVES: To improve platelet support for children with malignant diseases and to investigate the causes of abnormal bleeding in these patients. Investigations to define and characterize hemostatic abnormalities associated with malignancy should permit identification of mechanisms of platelet transfusion refractoriness and their appropriate management. Thus far, these studies have indicated the extensive consumption associated with acute leukemias in childhood with turnovers up to 6 times the normal and the high incidence of autoantibodies (57%) in acute lymphocytic leukemia. Studies to identify appropriate antithrombotic therapy to prevent consumption in patients with metastatic solid tumors has indicated that some of these patients are responsive to platelet function inhibition. In addition, the studies of the incidence of alloimmunization will define the risk for the development of this cause of platelet transfusion refractoriness. Further studies are needed to identify the potential value of antithrombotic therapy to reverse the consumptive process. Specifically what diseases may be responsive to therapy and what therapy (platelet function inhibition or anticoagulation) will be most helpful. Since platelet support in acute leukemia is one of the most difficult problems because of the development of refractoriness, further definition of the role of blood product administration as the cause of sensitization and its potential prevention with antileukemic drugs is needed. Therefore, samples of platelet antibody detection will be collected weekly through remission induction and maintenance regimens. Platelet donor selection for the alloimmunized recipient is essential. When patients become refractory to random donor platelet transfusions on the basis of alloimmunization, a crossmatch will be performed using the patients' serum or plasma and available family members or random platelet donors using the C14 labeled adenine release or radioimmunoassay techniques. In almost 50% of the newly diagnosed children with acute lymphoblastic leukemia, platelet antibodies are present at the onset. The significance of this finding is continuing under investigation.